Studies pertaining to the mechanisms of immunosuppression by C-type virus and by heteroantiserum raised against supernatants from lymph node cells primed against Class I alloantigens have high-lighted our research activities over the past period. These latter studies are leading to a greater understanding of the differentiation steps blocked by the immunosuppressive antiserum and have enabled us to define more precisely the criteria for monoclonal antibody isolation. Furthermore, the delineation of the targeted steps blocked by the antiserum enables us to determine what events are occurring upon priming by Class I disparate skin grafts. During the next year of support, we plan to identify a cell surface marker bound by the antiserum and whose binding/blocking is compromised by interleukin 1. This objective requires the production of monoclonal antibodies followed by specific immunoprecipitation of radiolabeled cell surface with the monoclonals and subsequent analysis by SDS-PAGE. The mechanism of immunosuppression by the C-type virus will be determined first via identification of the virus and terms of suppression. The questions that we will ask include whether suppression is mediated by a viral protein or if there is a specific infectivity of a T-cell subset. Furthermore, an analysis of the effects of this virus on mice will be undertaken in appropriate containment facilities. (HF)